Quick, Armand J.
October 1956
Angiology;Oct1956, Vol. 7 Issue 5, p419
Academic Journal
The escape of preformed thromboplastin from injured tissue, especially of the walls of blood vessels, brings about the production of a small amount of thrombin and the formation of a clot at the site of injury. On retraction a serum rich in nascent thrombin is expressed which, if the circulation is sluggish, brings about the formation of a second clot attached to the primary thrombus. The growth of the thrombus depends on clot retraction; consequently, the factors that increase this process accentuate the thrombotic tendency. The principal causes of increased clot retraction are thrombocytosis, decreased plasma fibrinogen, anemia, and increased thrombin generation. Their clinical implications are discussed. Intravascular clotting initiated by the blood itself occurs from massive hemolysis. A potent clotting factor similar to the one contained in the platelets is liberated from lysed erythrocytes. It reacts with the plasma clotting factors to form thrombin. As a result defibrinogenation, a reduction in prothrombin, platelets and other clotting agents, occurs but massive thrombosis is absent.


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